the pathophysiology of aortic stenosis can be explained from the following equation;

wall stress = (Pressure)x(heart radius)/muscle mass

since the aorta is narrowed, the pressure required for the Left Ventricle, LV to maintain a constant cardiac output is increased. this is turn will also increase the stress (pressure) that is absorb by the walls of the blood vessels (the body does not want this to happen as increase wall stress will damage the vessels). therefore as a compensation mechanism,the muscle mass of the LV will increase over a period of time (LV hypertrophy). increase muscle mass (LV hypertrophy) will reduce the compliance of the LV (LV is thick, so it is harder to expand). as compliance is reduced the end diastolic pressure will rise. the pressure required for the left atrium, LA to pump blood into the LV will also increase. as time goes, the LA will also become hypertrophied leading to an increase pressure in the pulmonary arteries. increase pressure of the pulmonary arteries will then causes pulmonary edema (fluid leakage - increase filtration). patient will show symptoms of breathlessness. as this condition progress, the heart is unable to increase the muscle mass of the LV anymore. from here, the LV will start to dilate and the patient will have cardiomegaly. ultimately, this will progress into left heart failure. the patient's condition may also lead to ride heart failure (if left untreated).

the concept is the same for hypertension.

some other stuff:
* LA hypertrophy may also lead to atrial fibrillation